A thalamic reticular networking model of consciousness

<p>Abstract</p> <p>[Background]</p> <p>It is reasonable to consider the thalamus a primary candidate for the location of consciousness, given that the thalamus has been referred to as the gateway of nearly all sensory inputs to the corresponding cortical areas. Interestingly, in an early stage of brain development, communicative innervations between the dorsal thalamus and telencephalon must pass through the ventral thalamus, the major derivative of which is the thalamic reticular nucleus (TRN). The TRN occupies a striking control position in the brain, sending inhibitory axons back to the thalamus, roughly to the same region where they receive afferents.</p> <p>[Hypotheses]</p> <p>The present study hypothesizes that the TRN plays a pivotal role in dynamic attention by controlling thalamocortical synchronization. The TRN is thus viewed as a functional networking filter to regulate conscious perception, which is possibly embedded in thalamocortical networks. Based on the anatomical structures and connections, modality-specific sectors of the TRN and the thalamus appear to be responsible for modality-specific perceptual representation. Furthermore, the coarsely overlapped topographic maps of the TRN appear to be associated with cross-modal or unitary conscious awareness. Throughout the latticework structure of the TRN, conscious perception could be accomplished and elaborated through accumulating intercommunicative processing across the first-order input signal and the higher-order signals from its functionally associated cortices. As the higher-order relay signals run cumulatively through the relevant thalamocortical loops, conscious awareness becomes more refined and sophisticated.</p> <p>[Conclusions]</p> <p>I propose that the thalamocortical integrative communication across first- and higher-order information circuits and repeated feedback looping may account for our conscious awareness. This TRN-modulation hypothesis for conscious awareness provides a comprehensive rationale regarding previously reported psychological phenomena and neurological symptoms such as blindsight, neglect, the priming effect, the threshold/duration problem, and TRN-impairment resembling coma. This hypothesis can be tested by neurosurgical investigations of thalamocortical loops via the TRN, while simultaneously evaluating the degree to which conscious perception depends on the severity of impairment in a TRN-modulated network.</p

Performance studies of the CMS strip tracker before installation

Peer reviewe

Role of L-type calcium-channel modulation in nonconvulsive epilepsy in rats

Contains fulltext : 28624.pdf (publisher's version ) (Open Access)Old male Wistar rats spontaneously showing hundreds of spike-wave discharges daily were used to investigate the role of calcium ions in nonconvulsive epilepsy. The effects of the L-type calcium channel blocker nimodipine and the L-type channel opener BAY K 8644 on number and duration of these spike-wave discharges were investigated. In rats aged 84-94 weeks standard EEG electrodes were chronically implanted; animals were allowed to recover for 10 days. After a baseline registration, nimodipine 2.2, 8.8, and 35.2 mg/kg or BAY K 8644 in dosages of 0.12, 0.47, and 1.88 mg/kg was administered. A control group received the solvent. EEG recordings were made to evaluate drug effects. The highest dose of nimodipine increased the number of spike-wave discharges, whereas BAY K 8644 reduced the number of spike-wave discharges dose dependently. The highest dose of BAY K 8644 also induced fatal convulsions in 3 animals. Our results demonstrate that the L-type calcium antagonist nimodipine facilitates spike-wave discharges and that the L-type calcium agonist BAY K 8644 protects against these discharges, in contrast to previous results suggesting that calcium channel blockers act as antiepileptic drugs (AEDs) and that calcium channel openers act as convulsants. Our results are a further example of the different pharmacologic profile of convulsive and nonconvulsive epilepsy and are also in contrast to what has been described for T-type calcium channel modulation. We therefore propose that modulation of L-type and T-type calcium channels have opposite effects in nonconvulsive epilepsy